 |
| Image Credit: Pixabay |
Authors: Victoria Weston, MD; Kevin Bajer, PharmD; and Randy Orr, MD
Northwestern University
Originally Published: Modern Resident, June/July 2013
The focus of this critical care pearl is to discuss the use of bicarbonate drips for severe metabolic acidosis, as well as alternative options, which are available. Given the current nature of medication shortages, it is valuable to learn about the alternative options available for use in some of our most critically ill patients.
When approaching a patient with metabolic acidosis, it is important to consider the cause of their acidosis (e.g., increased generation of acids as in lactic acidosis, ketoacidosis and ingestions vs. loss of bicarbonate or decreased acid excretion). As this is a relatively broad topic, this critical care pearl will focus on the treatment of lactic acidosis, as treatment of ingestions may vary with the substance ingested.
Bicarbonate infusion is appropriate for use in severe metabolic acidosis as a temporizing measure while concurrently treating the underlying cause, which is most commonly septic shock in the medical intensive care unit. The threshold for initiating treatment remains debatable but typically is pH<7.1.
There are several methods to calculate the bicarbonate deficit to guide infusion rate for repletion; two methods are shown below:
Method 1:
Bicarbonate volume of distribution (HCO3 Vd) = (0.4 + 2.6/measured HCO3) – ideal body weight
Ideal body weight: Males: 50 + 2.3 (height (in) – 60) OR Females: 45.5 + 2.3 (height (in) – 60)
HCO3 deficit (mEq) = HCO3 Vd x (desired HCO3* – measured HCO3)
*typically 10-15
Method 2:
HCO3 deficit (mEq) = 0.6 x wt (kg) x (15* – measured HCO3)
*Here, 15 is chosen as the end-point goal
To choose a rate, the bicarbonate deficit should be divided with half of the deficit repleted within the first 4 hours. Bicarbonate drips are provided as sodium bicarbonate 150mEq Dextrose 5% 1000mL. In a pinch, some physicians will choose an initial infusion rate of 150mEq run over 6 hours since this will provide an adequate replacement rate for most patients. Titration of further replacement should be guided by subsequent ABGs.
Of note, use of bicarbonate to correct metabolic acidosis requires adequate ventilation to release the CO2 generated. Potential risks and consequences of use include paradoxical CSF acidosis, hypernatremia, local tissue acidosis in cases of poor circulatory perfusion and diminished ionized calcium.
Given the current national sodium bicarbonate shortage, sodium acetate has been utilized more frequently as a therapeutic substitution. Acetate is metabolized systemically to bicarbonate on an equimolar basis when the body’s acid-base balance is altered as a result of bicarbonate deficiency (metabolic acidosis). To form bicarbonate, acetate is slowly hydrolyzed to carbon dioxide and water, which are then converted to bicarbonate by the addition of a hydrogen ion. These conversions take place primarily in the liver. Thus, the actions of sodium acetate mimic those of sodium bicarbonate in patients with intact hepatic function but should NOT be given as an IV push. Sodium acetate is not an appropriate choice for patients without a bicarbonate deficit (i.e., patients requiring urinary alkalinization). There are other alternative options such as carbicarb and THAM; however, these have been less frequently used at our institution.
The following indications should always receive sodium bicarbonate:
- High dose methotrexate patients
- Liver transplant patients
- Cardiac surgery patients
- Salicylate overdose patients
References:
1. Forsythe SM, Schmidt GA. Sodium bicarbonate for the treatment of lactic acidosis. Chest. 2000;117(1):260.
2. Kurtz I. Acid-Base Case Studies. 2nd Ed. Trafford Publishing (2004); 68:150
3. Marino PL. ICU book. 3rd Ed. Philadelphia:Lippincott, Williams, and Wilkins (2007); 551-553.